Activated ras oncogenes have been shown to confer the metastatic phenotype upon different non-neoplastic and benign neoplastic cell types. We have evaluated the effect of amplified expression of v-H-ras in an NIH/3T3 line, 433, which contains the ras under a transcriptional control of the glucocorticoid-sensitive mammary tumor virus long terminal repeat. Thus, treatment with a glucocorticoid, such as dexamethasone for 6 days, results in a 20-fold increase in P21 synthesis, and simultaneously suppresses the proteolytic activity of the 433 cells. The untreated 433 cells produced experimental metastases but not spontaneous metastases in nude mice. However, after dexamethasone treatment, the lung colonizing capacity was decreased two- to three-fold. These data show that amplification of expression of the ras gene under the control of a glucocorticoid promoter does not augment the metastatic capacity of the ras transfected cells.